Evidence map›Paper›PMID 28157223›Full record

ArticleEye (London, England)2017

Novel variants in PAX6 gene caused congenital aniridia in two Chinese families.

R Zhang, S Linpeng, X Wei, H Li, Y Huang, J Guo, Q Wu, D Liang, L Wu

Open access · bronzeAbstract read
In one paragraph

Article in Eye (London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Epistasis between Pax6Gene therapy · 2018
    Article
  7. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

R ZhangState Key Laboratory of Medical Genetics, Central South University, Changsha, China.
S LinpengState Key Laboratory of Medical Genetics, Central South University, Changsha, China.
X WeiState Key Laboratory of Medical Genetics, Central South University, Changsha, China.
H LiState Key Laboratory of Medical Genetics, Central South University, Changsha, China.
Y HuangState Key Laboratory of Medical Genetics, Central South University, Changsha, China.
J GuoState Key Laboratory of Medical Genetics, Central South University, Changsha, China.
Q WuHunan Jiahui Genetics Hospital, Changsha, China.
D LiangState Key Laboratory of Medical Genetics, Central South University, Changsha, China.
L WuState Key Laboratory of Medical Genetics, Central South University, Changsha, China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PurposeTo reveal the underlying genetic defect in two four-generation Chinese families with aniridia and explore the pathologic mechanism.MethodsFull ophthalmic examinations were performed in two families with aniridia. The PAX6 gene was directly sequenced in patients of two families, and the detected variants were screened in unaffected family members and two hundred unrelated healthy controls. Real-time quantitative PCR was used to explore pathologic mechanisms of the two variants.ResultsAniridia, cataract, and oscillatory nystagmus were observed in patients of the two families. In addition, we observed corneal opacity and microphthalmus in family 1, and strabismus, left ectopia lentis, microphthalmus, and microcornea in family 2. Sanger sequencing detected a novel 1-bp duplication (c.50dupA) in family 1 and a novel 2-bp splice site deletion (c.765+1_765+2delGT) in family 2. Sequencing of cDNA indicated skipping of exon 9 caused by the splice site deletion, being predicted to cause a premature stop codon, as well as the duplication. The PAX6 mRNA significantly lower in patients with aniridia than in unaffected family members in both families, suggesting that the duplication and splice site deletion caused nonsense-mediated mRNA decay.ConclusionsOur study identified two novel PAX6 variants in two families with aniridia and revealed the pathogenicity of the variants; this would expand the variant spectrum of PAX6 and help us better understand the molecular basis of aniridia, thus facilitating genetic counseling.

Indexed as

MutationAdolescentAdultAniridiaChildDNA Mutational AnalysisFemaleHumansIncidenceMaleMiddle AgedPAX6 Transcription FactorPedigreeReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNAPAX6 protein, humanPAX6 Transcription FactorRNA

Identifiers

PMID28157223
PMCPMC5518831
OpenAlexW2585216146

What OpenQuestion holds

Textmetadata
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.